Modulation of food reward by adiposity signals

Figlewicz, Dianne P.; Naleid, Amy M.; Sipols, Alfred J.

doi:10.1016/j.physbeh.2006.10.008

Cited by 138 publications

(128 citation statements)

References 58 publications

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“…However, there is also a hedonic aspect to feeding and hedonic feeding will possibly involve dopaminergic mechanisms of reward [152,[361][362][363][364]. A functional link between hypothalamic energy-control mechanisms and the motivational aspect of feeding has been demonstrated by Helm et al [240].…”

Section: Serotonin and The Pharmacotherapy Of Obesitymentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

257

167

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Serotonin has been implicated in the control of satiety for almost four decades. Historically, the insight that the appetite suppressant effect of fenfluramine is linked to serotonin has stimulated interest in and research into the role of this neurotransmitter in satiety. Various rodent models, including transgenic models, have been developed to identify the involved 5-HT receptor subtypes. This approach also required the availability of receptor ligands of different selectivity, and behavioural techniques had to be developed simultaneously which allow differentiating between unspecific pharmacological effects of these ligands and 'true' 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 3 IntroductionWhat are the behavioural and physiological mechanisms that promote satiety? How is satiety defined? Satiety can be seen as a behavioural state which arises from food consumption and suppresses the initiation of eating for a particular period of time [1]. This description alone suggests a high degree of complexity as peripheral post-ingestive and post-absorptive signals need to be relayed to the brain where they are integrated with other signals to produce (or not) the behavioural state called satiety. The state of satiety is brought about a process called satiation, where sensory, cognitive and early post-ingestive mechanisms bring feeding to a halt and thus stopping a meal. Promoting satiation alone must not necessarily lead to reduced total food intake as the frequency of meals could be increased subsequently. Many peripheral and brain mechanisms have been identified that are involved in the expression satiety and it has been suggested that serotonin accelerates satiation and prolongs satiety [2]. In the following, we will review the role of serotonin in satiety in more detail 1 . The reader will see that, despite immense progress made during the last years, the field is still far from being resolved.As serotonin (5-Hydroxytryptamine; 5-HT) is a phylogenetically old neurotransmitter, various functions had time to evolve in different phyla, but maybe also in different species. 5-HT receptors exist in animal cells for millions of years and they are as old as adrenoreceptors ore some peptide receptors, possibly even older [5,6]. Even in invertebrates such as molluscs (Aplysia californica) and annelids (Hirudo medicinalis), 5-HT might functionally be related to food intake [7]. 5-HT is involved in feeding even in the honeybee where it has separate effects in the gut and in the insect brain [8]. In general, however, 5-HT seems rather to be involved in appetitive behaviours in invertebrates whereas it has more of a satiating effect in vertebrates [9]. In general, 5-HT neurons seem to be more extensively distributed throughout the body in lower animals than in higher animals including mammals where 5-HT neurones...

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Section: Serotonin and The Pharmacotherapy Of Obesitymentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

257

167

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“…This system is responsive not only to a variety of glutamatergic inputs from local (Dobi et al, 2010) and distal (Geisler et al, 2007) neuronal sources, but also to a number of state variables mediated by blood-borne factors including leptin (Figlewicz et al, 2003;Krugel et al, 2003;Hommel et al, 2006;Liu et al, 2011;Thompson and Borgland, 2013). Leptin is an endogenous inhibitor of food reward (Figlewicz et al, 2007;Domingos et al, 2011) that has both direct (Fulton et al, 2006a;Krugel et al, 2003;Leinninger et al, 2009;Davis et al, 2011;Domingos et al, 2011) and indirect (Leinninger et al, 2009) effects on brain reward function and that is depressed in heroin addicts (Housová et al, 2005) and fluctuates abnormally during craving for alcohol (Kiefer et al, 2005) or nicotine (al 'Absi et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Reciprocal Inhibitory Interactions Between the Reward-Related Effects of Leptin and Cocaine

You

Wang

Liu

et al. 2015

Neuropsychopharmacol

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Cocaine is habit-forming because of its ability to enhance dopaminergic neurotransmission in the forebrain. In addition to neuronal inputs, forebrain dopamine circuits are modulated by hormonal influences; one of these is leptin, an adipose-derived hormone that attenuates the rewarding effects of food-and hunger-associated brain stimulation reward. Here we report reciprocal inhibition between the rewardrelated effects of leptin and the reward-related effects of cocaine in rats. First, we report that cocaine and the expectancy of cocaine each depresses plasma leptin levels. Second, we report that exogenous leptin, given systemically or directly into the ventral tegmental area, attenuates the ability of cocaine to elevate dopamine levels in the nucleus accumbens, the ability of cocaine to establish a conditioned place preference, and the ability of cocaine-predictive stimuli to prolong responding in extinction of cocaine-seeking. Thus, whereas leptin represents an endogenous antagonist of the habit-forming and habit-sustaining effects of cocaine, this antagonism is attenuated by cocaine and comes to be attenuated by the expectancy of cocaine.

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“…However, the relative paucity of available data in humans (Benedict et al, 2008;Hallschmid et al, 2012;Jauch-Chara et al, 2012) and animals (Woods et al, 1979;McGowan et al, 1992;Air et al, 2002;Clegg et al, 2003Clegg et al, , 2006 at the moment does not permit sound conclusions on macronutrient-specific effects of brain insulin on eating behavior (for review see Kullmann et al, 2016;Lee et al, 2016). Animal research has indicated that the adiposity signals insulin and leptin can directly act on the brain reward circuitry to decrease the intake of particularly palatable foods (Figlewicz et al, 2007). Although at a first glance, the insulin-induced reduction in carbohydrate intake would fit with the assumption that intranasal insulin specifically reduces the intake of highly rewarding foods , sweet items as a food category were not differentially affected here.…”

Section: Discussionmentioning

confidence: 99%

Central nervous insulin administration before nocturnal sleep decreases breakfast intake in healthy young and elderly subjects

Santiago

Hallschmid

2017

Diabetologie und Stoffwechsel

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Peripheral insulin acts on the brain to regulate metabolic functions, in particular decreasing food intake and body weight. This concept has been supported by studies in humans relying on the intranasal route of administration, a method that permits the direct permeation of insulin into the CNS without substantial absorption into the blood stream. We investigated if intranasal insulin administration before nocturnal sleep, a period of reduced metabolic activity and largely absent external stimulation, affects food intake and energy turnover on the subsequent morning. Healthy participants who were either young (16 men and 16 women; mean age ± SEM, 23.68 ± 0.40 years, mean BMI ± SEM, 22.83 ± 0.33 kg/m 2 ) or elderly (10 men, 9 women; 70.79 ± 0.81 years, 25.27 ± 0.60 kg/m 2 ) were intranasally administered intranasal insulin (160 IU) or placebo before a night of regular sleep that was polysomnographically recorded. Blood was repeatedly sampled for the determination of circulating glucose, insulin, leptin and total ghrelin. In the morning, energy expenditure was assessed via indirect calorimetry and subjects were offered a large standardized breakfast buffet from which they could eat ad libitum. Insulin compared to placebo reduced breakfast size by around 110 kcal (1,054.43 ± 50.91 vs. 1,162.36 ± 64.69 kcal, p = 0.0095), in particular decreasing carbohydrate intake (502.70 ± 25.97 vs. 589.82 ± 35.03 kcal, p = 0.0080). This effect was not dependent on sex or age (all p > 0.11). Sleep architecture, blood glucose and hormonal parameters as well as energy expenditure were not or only marginally affected. Results show that intranasal insulin administered to healthy young and elderly humans before sleep exerts a delayed inhibitory effect on energy intake that is not compensated for by changes in energy expenditure. While the exact underlying mechanisms cannot be derived from our data, findings indicate a long-lasting catabolic effect of central nervous insulin delivery that extends across sleep and might be of particular relevance for potential therapeutic applications.

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Modulation of food reward by adiposity signals

Cited by 138 publications

References 58 publications

Serotonin controlling feeding and satiety

Serotonin controlling feeding and satiety

Reciprocal Inhibitory Interactions Between the Reward-Related Effects of Leptin and Cocaine

Central nervous insulin administration before nocturnal sleep decreases breakfast intake in healthy young and elderly subjects

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